Mutations in SLC4A11 a member of the family of solute linked transporters, cause CHED2 (recessive congenital hereditary endothelial dystrophy) and late onset Fuchs Endothelial corneal dystrophy (FECD) in humans. Very limited research literature suggests that this gene codes for a Na- dependent bicarbonate transporter (BTR1) or borate transporter (NaBC1). This suggests that SLC4A11 codes for a protein that is part of the corneal endothelial fluid pump or a new transporter involved in regulating intracellular borate concentrations. Our preliminary data suggests that borate can be a cellular anti- oxidant. In this revision application we propose experiments to determine the type of transport that NaBC1 performs and whether its expression can affect intracellular borate concentrations, cell survival, and reactive oxygen species levels in corneal endothelial cells. Determining the function of NaBC1 is important for understanding its role in normal corneal endothelial function and the role it has in these corneal dystrophies. PUBLIC HEALTH RELEVANCE: Corneal endothelial dystrophies, Fuchs and CHED2, result in loss of corneal endothelial cells, corneal edema and poor vision. This project examines the role of a newly described gene SLC4A11 that has mutations associated with these dystrophies.